heart med 2

Question 1

Management
of NSTE-ACS
and ACS (MI)
Aim

Answer 1

of treatment is to stabilise the patient,
treat the lesion and slow progression of
atherosclerosis and prevent future events

Question 2

The gold standard treatment for STEMI

Answer 2

is revascularization with primary percutaneous
coronary intervention within 2 hrs. Where
this is not available treatment to dissolve the
clot is thrombolysis

Question 3

Management
of NSTE-ACS
and ACS (MI) drugs

Answer 3

Anticoagulant therapy
Thrombolytics agents
Antiplatelet therapy
Morphine
ACE inhibitors

Question 4

Antiplatelet therapy
Mechanism of action
Example
Adverse effects –

Answer 4

Mechanism of action
Aspirin as per previous slide
• P2Y12 inhibitors –blocks platelet receptors (P2Y12) inhibiting platelet aggregation by blocking
activation of the glycoprotein Iib/IIIa pathway
Example
• Clopidogrel
Adverse effects – severe neutropenia, TTP, haemorrhage
NB: Aspirin (previous slide) and P2Y12 inhibitors given immediately along with GTN (previous
slide) when patient presents with Chest pain

Question 5

Morphine

Answer 5

• Morphine has been used for analgesic effect and its vasodilator properties in ACS, however it has
been associated with an increased in-hospital risk of death (low grade confidence due to high risk
of bias in these studies). Morphine decreases the antiplatelet effect of P2Y12 inhibitors.

Question 6

Beta blockers

Answer 6

• Unless contra indicated they should be used to reduce infarct size and ischemia

Question 7

ACE inhibitors (

Answer 7

Long term management of ACS – improves survival and used for secondary prevention

Question 8

Anticoagulant therapy
Mechanism of action
Example
Adverse effects

Answer 8

• Combines with antithrombin III inactivating factor X and inhibiting conversion
of prothrombin to thrombin. If thrombin exists, inhibits further coagulation
(Heparin)
• Activates antithrombin inhibiting generation of thrombin, as well as
accelerating inhibition of factor Xa
Example
• Heparin, Enoxaparin (LMWH)
Adverse effects – haemorrhage, elevated liver enzymes (both), anaemia, nausea,
diarrhoea, fever (enoxaparin

Question 9

Thrombolytics agents
Mechanism of action
Example
Adverse effects

Answer 9

Mechanism of action
• Recombinant tissue plasminogen activator (r-tPA)) which acts on fibrin in
thrombus with little or no effect on circulation unbound plasminogen
(Dissolves existing clots)
• Re-perfuses occluded vessels in approximately 90 minutes in most patients
Example
• Alteplase, reteplase
Adverse effects –haemorrhage at IV site, minor or major bleeding, arrhythmias
(associated with reperfusion), hypotension

Question 10

Most antiarrhythmic drugs have two
actions that reduce abnormal electrical
activity

Answer 10

1. Suppress abnormal (ectopic)
pacemakers more than they do the
SA node
2. They increases the ratio for the
effective refractory period to action
potential durations
While they are divided into 4 classes,
many of them have properties of more
than one class

Question 11

Management of Arrhythmias/dysrhythmias

Answer 11

Class I
Class II
Class III
Class IV

Question 12

Class I

Management of Arrhythmias/dysrhythmias

Answer 12

Sodium channel blockers
•Act mainly by blocking sodium channels (depressing impulse conduction).
•Can also suppress automaticity by raising the membrane potential threshold required for delayed afterpolarizations
to trigger action potentials
Side effects – arrhythmias, other side effects depend on subclass and range from N & V, syncope, tinnitus, anxiety,
insomnia, increased sweating

Question 13

Class II

Answer 13

Beta blockers
• Used for rate control in arrhythmias
• Reduce the conduction of the atrial impulse through the AV node
Side effects – as previously discussed

Question 14

Class III

Answer 14

Potassium channel blockers
•Prolongs action potential duration and hence refractory period of atrial, nodal and ventricular tissues
•Increases coronary blood flow by vasodilation
•Suppresses ectopic pacemaker
Side effects – Bradycardia, cardiac failure and cardiac arrest. MANY cumulative adverse effects. Pulmonary fibrosis,
hypo and hyperthyroidism, liver dysfunction, photosensitivity , smurf syndrome, and peripheral neuropathy. It has a
very long half life (average 58 days)

Question 15

Class IV

Answer 15

Calcium channel blockers
•Their blockage slows AV node depolarisation and conduction and also increases its refractory period
Side effects - headaches, dizziness, GI symptoms, palpitations, hypotension, exacerbation of angina, rash